Rhythmical Excitation of the Heart

 generating rhythmical electrical impulses to cause rhythmical contraction of heart muscle

 conducting impulses rapidly through the heart
 atria contract 1/6s ahead of ventricular contraction, allows filling ventricles before they
 allows portions ventricles to contract simultaneously, for effective pressure generation
 rhythmical and conductive system - susceptible to damage by heart disease- ischemia
 bizarre heart rhythm or abnormal sequence of contraction of the heart chambers

Specialized Excitatory and Conductive System of the Heart

 the sinus node (sinoatrial or S-A node), normal rhythmical impulse is generated
 the internodal pathways - conduct impulse from sinus node to atrioventricular (A-V) node;
 A-V node - impulse from atria is delayed before passing into the ventricles;
 A-V bundle - conducts the impulse from the atria into the ventricles;
 Left, right bundle branches of Purkinje fibers-conduct cardiac impulse to parts of ventricles

Sinus (Sinoatrial) Node

 small, flattened, ellipsoid strip of specialized cardiac muscle

 3 millimeters wide, 15 millimeters long, and 1 millimeter thick
 superior PL wall of right atrium below and lateral to opening of superior vena cava
 fibers have no contractile muscle filaments each 3 to 5 micrometers in diameter
 contrast to diameter of 10 to 15 micrometers for atrial muscle fibers
 sinus nodal fibers connect directly with the atrial muscle fibers
 any action potential spreads immediately into the atrial muscle wall

Automatic Electrical Rhythmicity of the Sinus Fibers

 Some cardiac fibers - self-excitation=automatic rhythmical discharge and contraction

 fibers of the heart’s specialized conducting system+including the fibers of the sinus node
 sinus node ordinarily controls the rate of beat of the entire

Mechanism of Sinus Nodal Rhythmicity.

 “resting membrane potential” of sinus nodal fiber 55 to -60 millivolts

 -85 to -90 millivolts for the ventricular muscle fiber
 cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions
 types of membrane ion channels
 fast sodium channels, (2) slow sodiumcalcium channels, and (3) potassium channels.
 opening 1/ 10,000ths
  rapid upstroke spike of the action potential observed in ventricular muscle
 “plateau” of the ventricular action potential - slow sodium-calcium channels 0.3 second
 opening of potassium channels --returns the membrane potential to its resting level
 difference in the function of these channels in the sinus nodal fiber
 “resting” potential—only -55 millivolts in the nodal
 at -55 millivolts, the fast sodium channels “inactivated”
 when membrane potential <= -55 millivolts for more than a few milliseconds, inactivation gates on the
inside of cell membrane that close fast sodium channels become closed
 only slow sodium-calcium channels can open and cause action potential
 atrial nodal action potential is slower to develop; after action potential occurs, return of the potential
to its negative state occurs slowly as well

Self-Excitation of Sinus Nodal Fibers.

 high Na concentration extracuu, + open sodium channels, Na from outside tend to leak inside
 “resting” potential gradually rises between each two heartbeats
 potential reaches threshold voltage -40 mV, Na-Ca channels activate, cause action potential
 inherent leakiness of sinus nodal fibers to Na, Ca ions causes their self-excitation
 Why not depolarized all the time?
 sodium-calcium channels close within 100 to 150 ms after opening
 at about the same time, K channels open
 influx of positive calcium and sodium ions through the sodium-calcium channels ceases
 K channels remain open for another few 1/10 s hyperpolarization -55 to -60 mV
 next few tenths of a second potassium channels close
 leaking sodium and calcium ions once again overbalance the outward flux of potassium ions

Internodal Pathways and Transmission of the Cardiac Impulse Through the Atria

 ends of sinus nodal fibers connect directly with surrounding atrial muscle fibers
 action potential spreads through atrial muscle mass and to A-V node
 atrial muscle 0.3 m/sec
 specialized conduction fibers 1 m/sec
 the anterior interatrial band-through the anterior walls of the atria to the left atrium
 3 small bands through ALP atrial walls terminate in A-V node; A, mid, P internodal pathways
 similar to even more rapidly conducting “Purkinje fibers”

Atrioventricular Node, and Delay of Impulse Conduction from the Atria to the Ventricles

 cardiac impulse does not travel from the atria into the ventricles too rapidly
 time for atria to empty their blood into ventricles before ventricular contraction begins
 A-V node and its adjacent conductive fibers that delay this transmission into the ventricles
 in the posterior wall of the right atrium immediately behind the tricuspid valve
 0.03 traveling through the internodal pathways to A-V node after its origin in sinus node
 0.09 delay in the A-V node
 0.04 in penetrating A-V bundle, fascicles through fibrous tissue separate atria from ventricles
 --gap junctions between successive cells in the conducting pathways

Rapid Transmission in the Ventricular Purkinje System

 from the A-V node through the A-V bundle into the ventricles
  functional characteristics that are quite the opposite of those of the A-V nodal fibers
 large fibers, 1.5 to 4.0 m/sec, x6 ventricular muscle x150 some A-V nodal fibers
 high level of permeability of the gap junctions at the intercalated
 very few myofibrils

One-Way Conduction Through the A-V Bundle

 inability, except abnormal, action potentials travel backward from the ventricles to the atria
 atrial muscle separated from ventricular muscle by a continuous fibrous barrier
 insulator prevent passage of cardiac impulse atrial ->ventricular muscle through other route
 abnormal muscle bridge-penetrate fibrous barrier-cardiac impulse re-enter atria=arrhythmia

Distribution of the Purkinje Fibers in the Ventricles—The Left and Right Bundle Branches.

 distal portion of A-V bundle downward in ventricular septum 5-15mm toward heart apex
 divides into left and right bundle branches - beneath the
 branch spread downward toward ventricle apex, progressively into smaller branches
 around each ventricular chamber
 back toward the base of the heart
 time the cardiac impulse enters the bundle -> reaches the terminations 0.03

Transmission of the Cardiac Impulse in the Ventricular Muscle

 0.3 to 0.5 m/sec, one sixth that in the Purkinje fibers

 cardiac muscle wraps around the heart in a double spiral
 fibrous septa between the spiraling layers
 impulse don’t go directly to surface but angulates toward surface along spiral directions
 transmission from endocardial to epicardial surface of ventricle requires another 0.03
 total transmission time from initial bundle branches to the last ventricular muscle 0.06

Control of Excitation and Conduction in the Heart

The Sinus Node as the Pacemaker of the Heart

 The A-V nodal fibers, not stimulated from outside, intrinsic rhythmical 40-60, Purkinje 15-40
 rate of the sinus node of 70 to 80 times per minute
 sinus node control the heart’s rhythmicity- faster discharge rate

Abnormal Pacemakers—“Ectopic” Pacemaker

 some other part of the heart develops a rhythmical discharge rate faster than of sinus node
 sometimes occurs in A-V node or in Purkinje fibers when one of these becomes abnormal
 Under rarer conditions, a place in the atrial or ventricular
  pacemaker transmission blockage sin node->A-V or in penetrating portion of A-V bundle

When A-V block occurs

 atria continue to beat at the normal rate of rhythm of the sinus node
 new pacemaker usually in Purkinje system 15 and 40 beats per minute after 5 to 20 seconds
 before the blockage, the Purkinje fibers had been suppressed by rapid sinus impulses
 person faints after the first 4 to 5 seconds Stokes-Adams syndrome

Control of Heart Rhythmicity and Impulse Conduction by the Cardiac Nerves: The Sympathetic and
Parasympathetic Nerves

The parasympathetic nerves (the vagi) are distributed mainly to the S-A and A-V nodes, to a lesser extent to the
muscle of the two atria, and very little directly to the ventricular muscle.

The sympathetic nerves, conversely, are distributed to all parts of the heart, with strong representation to the
ventricular muscle as well as to all the other areas.

Parasympathetic (Vagal) Stimulation Can Slow or Even Block Cardiac Rhythm and Conduction—“Ventricular
Escape.”

 acetylcholine be released at the vagal endings

 decreases the rate of rhythm of the sinus node
 decreases excitability of A-V junctional fibers between atrial musculature and A-V node
 Weak to moderate vagal stimulation -half normal rate;
 stop rhythmical excitation by sinus node; block transm from atria to ventricles through A-V
 The ventricles stop beating for 5 to 20 seconds, but then some point in the Purkinje fibers, usually in
the ventricular septal portion of the A-V bundle, develops a rhythm of its own and causes ventricular
contraction at a rate of 15 to 40 beats per minute. This phenomenon is called ventricular escape.

Mechanism of the Vagal Effects.

 acetylcholine increases permeability for K, allows rapid leakage out of conductive fibers
 increased negativity inside the fibers-> hyperpolarization
 In the sinus node, hyperpolarization decreases resting potential to -65 to -75 mV
 sodium and calcium leakage requires much longer to reach threshold potential for excitation
 In the A-V node, hyperpolarization impedes atrial fibers generate enough electricity

Effect of Sympathetic Stimulation on Cardiac Rhythm and Conduction.

 increases the rate of sinus nodal discharge 3x

 increases rate of conduction as well as level of excitability in all portions of the heart
 increases greatly the force of contraction of all the cardiac musculature 2x

Mechanism of the Sympathetic Effect.

 norepinephrine increases permeability of fiber membrane to Na, Ca ions

 more positive resting potential
 increased rate of upward drift toward threshold for selfexcitation, accel self-excitation
 In the A-V node and A-V bundles, increased sodium-calcium permeability easier for action
potential to excite conducting fiber bundles, decrease the conduction time
 exciting the contractile process of the myofibrils